Kent‐Braun, Jane A.

Under some conditions, intracellular oxygen tension (PO2) may decrease to the point where oxygen availability limits respiration. Information about this critical PO2 and its determinants in vivo is sparse. PURPOSE: To determine the critical PO2 of human skeletal muscle, and its relationship to cellular energy consumption. METHODS: Interleaved proton and phosphorus magnetic resonance spectroscopy were used to quantify deoxymyoglobin and phosphorous metabolites in the tibialis anterior muscle of 6 subjects during 15 minutes of leg ischemia. Critical PO2 was determined as the PO2 at the phosphocreatine inflection point during ischemia. The rate of ATP consumption was determined from the linear slope of PCr depletion following the inflection point. RESULTS: The time to PCr inflection point was 282 ± 112 s (mean±SE). The corresponding critical PO2 was 0.47±0.27 torr, with a range of 0.21–0.96. PO2crit was not associated with the resting rate of ATP consumption (r =0.17), but was directly correlated to the rate of myoglobin desaturation (r =0.93) and inversely correlated to the time required to reach the PCr inflection point (r = −0.74). CONCLUSION: These data suggest that the relatively wide range of PO2crit in these subjects is attributable to inter‐subject differences in the ability of the muscle to maintain ATP production in the face of an ischemic insult. Support NIH AG21094, K02 AG023582

Proton magnetic resonance spectroscopy was used to investigate the effect of ischemic contractions on human skeletal muscle oxygenation. PURPOSE: To determine if ischemia+contraction produces greater muscle deoxygenation than ischemia alone. METHODS: 5 men performed the following protocols in a 4 tesla magnet: P1) 10 min of ischemic rest, then 4 min of intermittent maximal isometric voluntary contractions (MVCs), and P2) 1 min of ischemic rest, then 3.4 min of intermittent MVCs and 5.6 min of ischemic recovery. Deoxymyoglobin (dMb) was normalized to the peak obtained during 10 min of ischemic rest. RESULTS: In P1, dMb reached a plateau during 10 min of ischemic rest and was not affected by contractions (102 ± 4.1%). In P2, dMb increased rapidly, followed by a plateau that tended to be lower than that obtained during ischemic rest (86.7 ± 2.32%, p = 0.063). During ischemic recovery, dMb gradually increased to the same level observed during resting ischemia (102 ± 4.2%). CONCLUSIONS: The addition of contractions after 10 min of ischemia does not result in further desaturation, suggesting that the muscle is already fully desaturated. Overall, these results validate the use of 10 min of resting ischemia to calibrate the dMb by MRS, and suggest that the observed plateaus in the dMb signal reflect inadequate oxygenation rather than mitochondrial inhibition by metabolite accumulation. Support NIH AG21094, K02 AG023582